Evidence map›Paper›PMID 23515290›Full record

ArticleEndocrinology2013

TGF-β effects on prostate cancer cell migration and invasion are mediated by PGE2 through activation of PI3K/AKT/mTOR pathway.

Baohan T Vo, Derrick Morton, Shravan Komaragiri, Ana C Millena, Chelesie Leath, Shafiq A Khan

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
17.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 199 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Ablation of prostaglandin ENature biomedical engineering · 2026
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  10. Metformin: A Dual-Role Player in Cancer Treatment and Prevention.International journal of molecular sciences · 2024
    Review
  11. Article
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  16. Article
  17. Article
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  19. Article
  20. Article

50 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Baohan T VoCenter for Cancer Research and Therapeutic Development, Clark Atlanta University, 223 James P. Brawley Drive, SW, Atlanta, Georgia 30314, USA.
Derrick Morton
Shravan Komaragiri
Ana C Millena
Chelesie Leath
Shafiq A Khan
Clark Atlanta University · USCenter for Cancer Research · US

Funding

THEORY OF PLANNED BEHAVIOR VS ETHNICITY /PHYSICAL ACTIVIG12RR003062 · NCRR · CLARK ATLANTA UNIVERSITY · PI BROWN, CARLTON B · 1985 to 2011
$15.5M
Research Initiative for Scientific Enhancement (RISE)R25GM060414 · NIGMS · CLARK ATLANTA UNIVERSITY · PI MUSEY, PAUL I. · 1999 to 2020
$13.7M
TRAINNING COREP20MD002285 · NIMHD · CLARK ATLANTA UNIVERSITY · PI CHAUDHARY, JAIDEEP · 2007 to 2016
$10.9M
Technologies/Resources for Core LaboratoriesG12MD007590 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2012 to 2018
$7.6M
NCRR NIH HHS G12 RR003062NIGMS NIH HHS 2R25GM060414NIGMS NIH HHS R25 GM060414NIMHD NIH HHS G12 MD007590NIMHD NIH HHS G12MD007590NIMHD NIH HHS P20 MD002285
6 · The paper itself

Abstract

TGF-β plays an important role in the progression of prostate cancer. It exhibits both tumor suppressor and tumor-promoting activities. Correlations between cyclooxygenase (COX)-2 overexpression and enhanced production of prostaglandin (PG)E2 have been implicated in cancer progression; however, there are no studies indicating that TGF-β effects in prostate cancer cells involve PGE2 synthesis. In this study, we investigated TGF-β regulation of COX-1 and COX-2 expression in prostate cancer cells and whether the effects of TGF-β on cell proliferation and migration are mediated by PGE2. COX-1 protein was ubiquitously expressed in prostate cells; however, COX-2 protein levels were detected only in prostate cancer cells. TGF-β treatment increased COX-2 protein levels and PGE2 secretion in PC3 cells. Exogenous PGE2 and PGF2α had no effects on cell proliferation in LNCaP, DU145, and PC3 cells whereas PGE2 and TGF-β induced migration and invasive behavior in PC3 cells. Only EP2 and EP4 receptors were detected at mRNA levels in prostate cells. The EP4-targeting small interfering RNA inhibited PGE2 and TGF-β-induced migration of PC3 cells. TGF-β and PGE2 induce activation of PI3K/AKT/mammalian target of rapamycin pathway as indicated by increased AKT, p70S6K, and S6 phosphorylation. Rapamycin completely blocked the effects of TGF-β and PGE2 on phosphorylation of p70S6K and S6 but not on AKT phosphorylation. PGE2 and TGF-β induced phosphorylation of AKT, which was blocked by antagonists of PGE2 (EP4) receptors (L161982, AH23848) and PI3K inhibitor (LY294002) in PC3 cells. Pretreatment with L161982 or AH23848 blocked the stimulatory effects of PGE2 and TGF-β on cell migration, whereas LY294002 or rapamycin completely eliminated PGE2, TGF-β, and epidermal growth factor-induced migration in PC3 cells. We conclude that TGF-β increases COX-2 levels and PGE2 secretion in prostate cancer cells which, in turn, mediate TGF-β effects on cell migration and invasion through the activation of PI3K/AKT/mammalian target of rapamycin pathway.

Indexed as

CarcinomaCell MovementDinoprostoneDrug Evaluation, PreclinicalEnzyme ActivationEnzyme InhibitorsHumansMaleNeoplasm InvasivenessPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProstatic NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesTransforming Growth Factor betaDinoprostoneEnzyme InhibitorsMTOR protein, humanPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTransforming Growth Factor beta

Identifiers

PMID23515290
PMCPMC3628025
OpenAlexW2001740655

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.